The absence of supplemental induction of neurotrophin receptors on the bronchial epithelia during bronchial asthma may lead to the epithelial denudation

Abstract

Bronchial asthma is characterized by airway inflammation, bronchial hyperresponsiveness, reversible bronchial obstruction, eosinophilia, and specific IgE response. Involved in this pathogenesis are neurotrophins such as nerve growth factor or brain-derived neurotrophic factor, which mediate their inflammatory effects through their receptors like tropomyosin-receptor kinases and pan-neurotrophin receptor p75. In addition, the induction of the above-mentioned mediators promotes increased surviving capacities for various cells of bronchial mucosa, which are in contact with noxious stimuli. In contrast to a wide variety of cellular populations, the denudation of local epithelia during bronchial inflammation, associated with potentiation of bronchial hyperresponsiveness mediated by subepithelial neuronal fibers is observed. In the context of these processes, bronchial epithelial cells show an increased neurotrophin synthesis, associated with decreased expression levels of relative receptors. This pattern contrasts again to other resident or emigrated cellular populations within bronchial tissue, which show both neurotrophin and neurotrophin receptor induction. It seems that apart from destructive abilities of specific or nonspecific noxious stimuli on the bronchial epithelia, the presence of depleted survival stimuli due to lack of neurotrophin receptors expression on the mentioned cellular population play a strategical role in epithelial destruction. This effect might be initiated by the asthmatic patient in order to provide airway hyperresponsiveness and thereby reduce the contact with harmful stimuli due to bronchial obstruction.